After delivering a pacing stimulation pulse to the atrium, it is important to detect the “evoked wave”, i.e., the depolarization wave induced by pacing the atrium to determine whether the stimulation pulse delivered was effective. This test (known as a “capture test”) is used to adjust the pacing stimulation pulse amplitude and/or pulse width. However, in the case of an atrial stimulation, the search for the evoked wave is particularly difficult. Indeed, not only is the amplitude of the evoked wave in the atrium much lower value than the amplitude of the evoked wave in the ventricle, but it also appears much earlier relative to the delivery of the stimulation pulse: the atrial evoked wave (P wave) starts approximately 10 ms after stimulation of the atrium and finishes at about 30 ms—whereas the evoked ventricular wave (R wave) is observed to start at about 60 ms after stimulation.
The very early atrial evoked wave is particularly mixed or even masked in the detection amplifier output of the transient electrical signal called “amplifier response,” which follows the electrical stimulation. This “amplifier response” is always present, whether the evoked wave is present or not. More specifically, to discharge the charges appearing at the heart/electrode interface after a stimulation, it is planned to release the stored energy by simultaneously disconnecting or “blanking” the detection circuits of the amplifier, typically for a duration of about 14 ms. Moreover, when the amplifier is reconnected to the poles of the electrode at the end of the blanking period, a transient rebound voltage occurs at the output of the amplifier, and persists a few milliseconds until the amplifier is completely desaturated.
It shall be understood that in these circumstances, it is very difficult to detect the presence of an evoked P wave, for example, as part of an atrial capture test.
EP 1 433 497 A1 and its counterpart U.S. Pat. No. 7,203,544 (ELA Medical) describe a technique to improve the response of the amplifier for atrial detection by a controlled inhibition of atrial detection circuits in order to search for post-stimulation spontaneous complexes after “micro-blanking”, the real “blanking” being activated later to allow the complete discharge of stored energy at the heart/electrode interface after the stimulation.
This technique of direct electrical measurement of evoked potentials produced by the atrium requires very precise control over the detection amplifier. It provides a definite improvement, but still does not guarantee safe detection of spontaneous complexes in all clinically feasible circumstances, given the variability of amplitudes, the instants of occurrence, etc., of the electrical potentials that are to be measured to detect the presence or absence of the evoked wave.
EP 1 407 800 A1 and its counterparts U.S. Pat. No. 7,349,737 and U.S. Pat. No. 7,483,745 (ELA Medical) describe another indirect way to detect the evoked atrial wave, by analysis of the intrinsic sinus rhythm of the patient and/or AV conduction delays of the patient's heart. Such indirect methods are, however, limited in their applicability and may particularly be in default in case of atypical cardiac events. For example, one method concerns pacing the atrium and assessing the presence of the conduction to ventricle via a second lead placed in the ventricle of the patient. But this method cannot be implemented in patients with complete atrioventricular block (which is, to be sure, a common problem justifying the initial implantation of a pacemaker). In general, the test function can be tricked by the occurrence of paroxysmal atrioventricular blocks in a patient who does not have the symptoms of a complete block.
The WO 2005/089866 A1 proposes a third approach, different from a direct electrical measurement of the depolarization potential on the atrium, and an indirect determination from the rhythm analysis and from the atrial and ventricular sequencing, which concerns measuring a mechanical characteristic, by detecting the atrial contraction from a signal representing the endocardiac acceleration delivered by an appropriate accelerometer sensor. Such a sensor may be present on the atrial lead or on another lead with a sensor, said lead being placed directly in the atrium or in another position to detect the signal of endocardiac acceleration (EA) signal representative of the contractions of the atrium.
In this third approach, the device, after atrial pacing, uses a functional signal—the EA signal—representative of the cardiac mechanics, instead of a signal originated from the electrical propagation of the depolarization wave. This mechanical signal can also be exploited as a complement of the electrical signal, as described in the US2007/0179541 A1 whose purpose is to measure and analyze the delay between the electrical detection and the mechanical detection of the atrial contraction.
WO2005/089866 A1 suggests to use the EA signal for various purposes such as optimization of the AV delay in the case of a dual chamber stimulation, optimization of the VV delay in the case of the biventricular stimulation for a therapy of Cardiac Resynchronization Therapy (CRT”), detection of the capture in a cardiac cavity, etc.
However, as for the electrical signal, the component of the EA signal corresponding to the atrial activity not only presents a much lower amplitude than in the case of the ventricle, but it also occurs much earlier, which renders its detection and analysis much more difficult. This is believed to be the reason why no technique based on the analysis of the atrial component of the EA signal procuring really exploitable results was proposed until now by the inventors, despite the interest of disposing of a signal directly reflecting the mechanical activity of the heart.